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Biomedical subjects

M Craighill

Publications and source records attributed to M Craighill.

4 recordsLinked to original sources
PubMed1994

Histologic correlates of vulvar human papillomavirus infection in children and young adults.

Two clinically important issues in the treatment of vulvar wartlike lesions are the histologic criteria for the recognition of human papilloma virus (HPV)-related lesions and the exclusion of lesions derived from cutaneous rather than genital HPV types. We analyzed a series of 70 biopsies from the vulva or distal vagina of 57 children and 13 young adults for HPV nucleic acids by polymerase chain reaction (PCR) amplification and typed the isolates following isotope labeling and restriction digestion (restriction fragment length polymorphism [RFLP] analysis). Lesions were classified as condyloma, suggestive of condyloma (papillary/verrucous architecture without koilocytotic atypia), or nonspecific epithelial alterations. Three observers independently agreed on the presence of papillary/verrucous architecture and koilocytotic atypia with a high degree of concordance (kappa = 0.74 and 0.71, respectively). By RFLP analysis, 77% of the lesions diagnosed as condyloma and 68% of those diagnosed as suggestive of condyloma contained HPV nucleic acids versus 9% of the nonspecific group. The HPV types identified were HPV 6 (67%), HPV 11 (17%), HPV 16 (3%), and unknown types (14%). No cutaneous HPV types were identified. Three patients with unknown HPV types had a history of sexual abuse, implying a genital source. These findings indicate that verrucopapillary external genital lesions, as defined in this report, are likely to be associated with HPV and that the vast majority contain genital HPV types irrespective of histologic presentation.

Adult↗
PubMed1987

Müllerian aplasia associated with maternal deficiency of galactose-1-phosphate uridyl transferase.

The activity and electrophoretic pattern of galactose-1-phosphate uridyl transferase (transferase), a key enzyme in galactose metabolism, were analyzed in four patients with Müllerian aplasia (Rokitansky-Küster-Hauser syndrome) and their mothers. Mothers of two of the patients had genetic variations of their transferase enzymes with activities below the normal range. Affected daughters from these two mothers also had genetic variations of the transferase enzyme. In one of the patients whose Müllerian aplasia had been diagnosed 15 years previously, premature ovarian failure developed. These case reports suggest a possible association between errors of galactose metabolism, Müllerian aplasia, and premature menopause--an association that is supported by a rodent model in which female offspring of mothers fed a high-galactose diet were born with reduced oocyte numbers and delayed vaginal opening.

Adult↗
PubMedDate not supplied

A clinical pathway for pelvic inflammatory disease for use on an inpatient service.

OBJECTIVE: (1) To create a guideline to improve care of adolescent patients diagnosed with pelvic inflammatory disease (PID); (2) to promote cost-effective, consistent care while minimizing delays and ensuring timely and appropriate use of laboratory tests and other interventions; and (3) to describe the process of the development and the implementation of a clinical pathway for PID. METHODS: The study involved the creation and piloting of a multidisciplinary, collaborative clinical pathway for uncomplicated PID on an inpatient service, and the development of a standardized form for analysis of demographics and variances from the pathway. The setting was an inpatient adolescent service at a children's hospital in an urban setting. All patients admitted with a clinical diagnosis of PID from April 1, 1993, to November 30, 1993, were followed up by means of the clinical pathway. All patients discharged with a diagnosis of uncomplicated PID in fiscal year 1992 (FY92: October 1, 1991, to September 30, 1992) were used as a comparison population. The main outcome measures included length of stay, charges per patient, timing of antibiotic administration, use of laboratory tests at admission and at 48 to 72 hours, and documentation of pathway variances. RESULTS: A clinical pathway was created by consensus during a period of several months. During implementation, 28 of 34 (82%) patients admitted by use of the pathway had a final diagnosis of PID; 23 of the 28 (82%) had uncomplicated PID. Variances from the pathway included missed rapid plasma reagins (RPRs) and laboratory tests that were not indicated. For uncomplicated PID, length of stay was reduced (p=.08) from a median of 4 days in FY92 (mean, 5.0 1 3.1 days; range, 2-15 days) to a median of 3 days in the study group (mean, 3.5 + 1.0 days; range, 2-4 days), with differences not reaching the level of significance. There were significantly more patients staying 5 days or longer in FY92 than in the study group (p<.03). Average charges per patient also decreased by 10% (median, $5,275 in FY92 to $4,919), although these results were not statistically significant. CONCLUSION: A clinical pathway for uncomplicated PID can be developed and implemented through a multidisciplinary, collaborative process, with ongoing use as a means of quality improvement and continuing education. Variances from the pathway highlight the need for ongoing education for health care providers. Downward trends in charges per patient and length of stay, although not significant, are encouraging; but they require longitudinal follow up with larger numbers of patients and analysis of outcomes.

Adolescent↗